Hot tumors are tumors caused by the environment, including several types of skin or lung cancer, and they emit an unusual amount of proteins. On the other hand, cold cancer tumors are those that appear following a genetic mutation in the so-called hereditary cancers, and they produce a healthy amount of proteins.

The so-called hot tumors are often more sensitive to immunotherapy than the cold tumors, without researchers so far being able to explain why.

A new study tried unlocking the mysteries of “tumor heterogeneity” which means the ability of a cancer cell to move, replicate, metastasize, and respond to treatment.

“Every tumor is different, so we’re studying how we can use tumor cell biology to treat more cancer patients,” says Ben Stanger, a professor from the Perelman School of Medicine in Pennsylvania, and the study’s leading author.

The research team found that the “hot” and “cold” character of a tumor is determined by information integrated into the cancer cells themselves.

“We have also identified that cold tumor cells produce a compound called CXCL1, which eventually leads to insensitivity to immunotherapy,” the study reads.

By removing CXCL1 from cold tumors, scientists were able to transform them into hot tumors in mice, making them more sensitive to immunotherapy.

Before that, none of the mice with cold tumors survived their cancers despite receiving a combination of chemotherapy and immunotherapy. On the other hand, of the 26 mice with hot tumors, 20 survived for more than six months.

That discovery increased hopes of an improvement in survival rates in mice affected by cold tumors. The scientists hope that this procedure would eventually help human patients with hereditary cancers, such as some breast and ovarian cancers, familial adenomatous polyposis (FAP), von Hippel-Lindau syndrome, or medullary thyroid cancer, among others.